The study by Kobayashi et al. showed that VASH1-induced tubulin detyrosination inhibited angiogenesis by impairing the endocytosis and trafficking of VEGF-receptor 2 (VEGFR2) in endothelial cells [68], which was contrary to our findings that VASH2-induced tubulin detyrosination promoted LUSC tumor growth by facilitating the EGFR recycling in cancer cells. Here, EGFR is linked to neoplasm.